Researchers from universities in Italy, Brazil and the United States did a study comparing resistance trained (RT) athletes who engaged in intermittent fasting (16/8) with RT athletes who ate normally.

The experiment ran for 8 weeks and the study was published in the Journal of Translational Medicine in October, 2016. You can read it here.

My purpose with this post is to give some thoughts about this study. I also did a video review.

RT in IF versus Normal Diet

One thing I liked about this study was in the introduction section, noting the difference between fasting and starvation. A common mistake that I often see in the literature (and anecdotally) is to put these two under the same ‘hood’:

“In contrast to fasting, starvation is a chronic nutritional deficiency that is commonly incorrectly used as a substitute for the term “fasting”. Starvation could also refer to some extreme forms of fasting, which can result in an impaired metabolic state and death.”[1]

To enter the study, athletes had to have been doing RT continuously for at least 5 years, with 3-5 days of training per week. They also had to have been life-long steroid free. I don’t get how they validated for their steroid status…

The training protocol involved 3 sets of 6–8 repetitions at 85–90 % 1-RM, and repetitions were performed to failure (i.e. the inability to perform another repetition with correct execution) with 180 s of rest between sets and exercises [36]. Te technique of training to muscular failure was chosen because it is one of the most common practices for body builders, and it was a familiar technique for the subjects.

Training sessions were performed between 4:00 and 6:00 p.m. Subjects were not allowed to perform other exercises other than those included in the experimental protocol.” [1]

Findings

They observed a reduction in fat mass with preservation of lean mass in the IF (TRF) group, with a concurrent decrease in testosterone and IGF-1 compared to the ND group:

“After 8 weeks, a significant decrease in fat mass was observed in the TRF group (-16.4 vs -2.8 % in ND group), while fat-free mass was maintained in both groups (+0.86 vs +0.64 %). Total testosterone and IGF-1 decreased significantly in TRF after 8 weeks while no significant differences were detected in ND. Blood glucose and insulin levels decreased significantly only in TRF subjects and conformingly a significant improvement of HOMA-IR was detected.” [1]

Interestingly, lower T and IGF-1 did not seem to negative impact lean mass. By their reasoning, this situation could be beneficial from a healthspan perspective:

“Decrease the activity of the IGF-1 axis could be a desirable target for reducing cancer risk [69], but it is also well known that the activation of the IGF-1/AKT/mTOR (insulin-like growth factor-1/protein kinase B/mammalian target of rapamycin) pathway is one of the keys for muscular growth. In addition to altering IGF-1, fasting can promote autophagy [28], which is important for optimal muscle health [70].” [1]

They hypothesize that the higher fat loss in the TRF group could be due to their higher adiponectin levels influencing AMPk and PGC1-alpha signaling:

It is notable that in the present study, the differences in adiponectin between groups remained even when normalized relative to body fat mass, whereas the significant decrease of leptin (that might be considered a unfavorable factor for fat loss) was no longer significant when normalized for fat mass. Other hypothesis is an enhanced thermogenic response to epinephrine [54] or an increase in REE [55] after brief periods of fasting, but our preliminary data didn’t support this point.” [1]

TRF group also experience a decrease in T3 levels with no changes in TSH or RER. This is different to what’s been hypothesized by other researcher: that fasting and lower T3 reduces RER. However, it should not be surprising to see no change in RER given that the overall energy intake in the TRF subjects was not at deficit.

“Although a reduction in T3 was observed in the IF group, no changes in TSH or resting energy expenditure were observed. The observed reduction in RR in the TRF group indicates a very small shift towards reliance on 9fatty acids for fuel at rest, although a significant statistical interaction for RR was not present.” [1]

Now, to the pitfalls and potential limitations:

Different dietary protocols (low-carb-high-fat vs. low-fat-high-carb) and different meal timing strategies (feeding window earlier, training later?, fasted training?, etc) could have affected subjects’ responses to RT differently. Such different strategies could have also elicited different blood biomarker results.

One of the biggest limitations of this experiment is that macros and energy intake were assessed based on interview – so, as per the recalling of the subjects:

“Because of the limitations of this method, it is possible that differences in energy or nutrient intake between groups could have existed and played a role in the observed outcomes.” [1]

Thus, I would not derive any strong take-away message from this study alone as there is no accurate dietary picture. Further studies and replicability are thus obligates…